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Tetanus

Chapter 157 | Part 5: Infectious Diseases

KEY CLINICAL POINTS

  • Tetanus is a preventable disease caused by Clostridium tetani neurotoxin, characterized by skeletal muscle spasms and autonomic dysfunction.
  • Global neonatal tetanus deaths decreased significantly due to WHO/UNICEF programs, but ~25,000 neonatal deaths occurred in 2018.
  • Unvaccinated individuals and those with incomplete vaccination are at highest risk, with ~50,000 annual global deaths.
  • Management includes wound debridement, antitoxins (HTIG preferred), benzodiazepines, and ventilatory support for severe cases.
  • Ablett classification and Tetanus Severity Score (TSS) guide prognosis, with TSS ≥ 8 predicting mortality (sensitivity 66%, specificity 91%).

1. DEFINITION & OVERVIEW

Tetanus is a neurologic infection caused by Clostridium tetani neurotoxin. Diagnosis is clinical with limited laboratory confirmation. Neonatal tetanus is defined by WHO as tetanus in infants with normal suck/cry ability in first 2 days but loss of these functions between days 3–28.

Table 157-1: Ablett Classification of Severity of Tetanus

GRADE SEVERITY SYMPTOMS
I Mild Mild trismus, general spasticity, no respiratory compromise, no spasms, no dysphagia
II Moderate Moderate trismus, rigidity, short spasms, mild dysphagia, moderate respiratory involvement, respiratory rate >30 breaths/min
III Severe Severe trismus, generalized rigidity, prolonged spasms, severe dysphagia, apneic spells, pulse >120 beats/min, respiratory rate >40 breaths/min
IV Very severe Grade 3 with autonomic dysfunction

1.1 Clinical Classification

Tetanus is categorized into generalized (most common), localized, cephalic, and neonatal forms. Neonatal tetanus presents with inability to suck, poor feeding, and generalized spasms.

1.2 Diagnostic Criteria

Diagnosis is based on clinical findings. CDC defines probable tetanus as acute illness with muscle spasms/hypertonia in absence of more likely diagnoses. Neonatal tetanus is diagnosed by WHO criteria.

2. EPIDEMIOLOGY

Global tetanus incidence has decreased with improved vaccination, but ~50,000 deaths occur annually. In 2022, 28 cases were reported in the US. Neonatal tetanus deaths decreased to ~25,000 in 2018. Risk factors include lack of vaccination, diabetes, IV drug use, and poor wound care.

2.1 Demographics

In the US (2009–2017), 64% of cases occurred in 20–64 years, 13% <20 years. Neonatal tetanus: 3 cases reported in 2009–2017. Older children/adults: estimated 30,000–62,000 deaths in 2015.

2.2 Risk Factors

Unvaccinated individuals, incomplete vaccination, lack of booster shots (>10 years), deep wounds, and poor wound care (e.g., unhygienic umbilical cord cutting).

3. ETIOLOGY & PATHOPHYSIOLOGY

C. tetani is an anaerobic, spore-forming gram-positive rod. Spores survive in environment and enter through wounds/umbilical stump. Toxin (tetanospasmin) undergoes retrograde transport to CNS, blocking inhibitory interneurons and causing hyperexcitability.

Table 157-2: Tetanus Severity Score (TSS)

VARIABLES SCORE
Age (year) £70: 0; 71–80: 5; >80: 10
Time from first symptom to admission (days) £2: 0; 3–5: –5; >5: –6
Difficulty breathing on admission No: 0; Yes: 4
Coexisting medical condition Fit and well: 0; Minor illness: 3; Moderately severe: 5; Immediately life-threatening: 9
Entry sites Internal/injection: 7; Other: 0
Highest systolic blood pressure (mmHg) £130: 0; 131–140: 2; >140: 4
Highest heart rate (beats/min) £100: 0; 101–110: 1; 111–120: 2; >120: 4
Lowest heart rate (beats/min) £110: 0; >110: –2
Highest temperature (°C) £38.5: 0; 38.6–39: 4; 39.1–40: 6; >40: 8

3.1 Toxin Mechanism

Tetanus toxin (150-kDa protein) cleaves into heavy (100-kDa) and light (50-kDa) chains. Light chain (zinc-dependent endopeptidase) cleaves VAMP2, preventing neurotransmitter release and causing unregulated motor neuron activity.

3.2 Autonomic Effects

Toxin affects autonomic nervous system, causing cardiovascular instability, sweating, and gastrointestinal stasis. Severe cases show elevated catecholamine levels.

4. CLINICAL FEATURES

Clinical manifestations include trismus (lockjaw), muscle rigidity, generalized spasms, and autonomic disturbances. Neonatal tetanus presents with inability to suck, poor feeding, and spasms. Cephalic tetanus may cause aspiration or airway obstruction.

4.1 Presentation by Type

Generalized (most common): muscle rigidity, spasms. Localized: isolated muscle spasms. Cephalic: pharyngeal/laryngeal spasms. Neonatal: inability to suck, generalized spasms.

4.2 Complications

Respiratory failure, cardiovascular instability, sepsis, and long-term neurological sequelae (e.g., cerebral palsy, learning disabilities).

5. DIFFERENTIAL DIAGNOSIS

Conditions mimicking tetanus include strychnine poisoning, dystonic drug reactions, stiff-person syndrome, neuroleptic malignant syndrome, and peritonitis. Abdominal rigidity in tetanus is continuous vs. acute abdomen.

5.1 Key Differentiators

Continuous abdominal rigidity vs. acute abdomen; pharyngeal spasms with aspiration risk; autonomic instability (fluctuating BP/HR).

6. INVESTIGATIONS & DIAGNOSIS

Diagnosis is clinical. Laboratory tests include serum antitetanus IgG (levels >0.1 IU/mL are protective). PCR/RPA for tetanus neurotoxin gene detection is emerging. Confirmatory tests are limited.

6.1 Diagnostic Tests

Serum antitetanus IgG (ELISA), PCR/RPA for toxin gene, and bioassay for circulating toxin (not routinely performed).

7. MANAGEMENT & TREATMENT

Immediate wound debridement, antitoxins (HTIG preferred), antibiotics (metronidazole), benzodiazepines, and ventilatory support. Sedation with propofol or midazolam may be required. Neuromuscular blockers used in severe cases.

7.1 Antitoxin Therapy

Human tetanus immunoglobulin (HTIG: 500–5000 IU IM) preferred over equine antitoxin. Intrathecal HTIG showed no benefit in trials.

7.2 Pharmacologic Management

Metronidazole (500 mg IV q6h x7d), benzodiazepines (diazepam 10–20 mg IV q2–4h), midazolam, or propofol for sedation. Magnesium sulfate for autonomic control.

7.3 Airway Management

Tracheostomy preferred for severe cases. Mechanical ventilation required for respiratory failure. Sedation with caution in elderly/liver disease.

8. PROGNOSIS & COMPLICATIONS

Mortality is 10–20% globally, with higher rates in severe cases. Prognosis depends on incubation period (shorter = worse), TSS ≥ 8 predicts mortality. Complications include respiratory failure, sepsis, and long-term neurological sequelae.

8.1 Predictive Factors

Short incubation period, rapid disease progression, and TSS ≥ 8 (sensitivity 66%, specificity 91%).

9. SPECIAL CONSIDERATIONS

Vaccination is key prevention. CDC recommends DTP3 vaccination (94% coverage in 2022). Maternal immunization reduces neonatal tetanus by 94%. Booster doses every 10 years required for immunity.

9.1 Prevention

Safe delivery, hygienic umbilical cord care, maternal vaccination, and wound management. Catch-up schedules for incomplete vaccination.

9.2 Vaccination Schedules

Infants: 2, 4, 6 months, 15–18 months, 4–6 years. Adolescents: 11–12 years. Adults: every 10 years. High-risk areas: primary course for women of childbearing age.

10. KEY POINTS & CLINICAL PEARLS

  1. Tetanus is a medical emergency requiring immediate antitoxin and ventilatory support. 2. HTIG is preferred over equine antitoxin. 3. TSS ≥ 8 predicts mortality. 4. Vaccination prevents 94% of neonatal tetanus. 5. Magnesium sulfate and sedatives are critical for autonomic control.